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Pharmacotherapy 2/3 > CV Overview > Flashcards

CV Overview Flashcards

1
Q

deoxygenated blood leaves the lungs via the

A

pulmonary artery

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2
Q

which layer is the inner most layer of arteries and veins?

A

tunica intima

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3
Q

What is a consequence of angiotensin II on angiotensin I receptors?

A

vasoconstriction
increase glomerular filtration rate
increase antidiuretic hormone (ADH)
aldosterone stimulation

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4
Q

What is a consequence of chronic aldosterone production?

A

myocardial fibrosis
endothelial dysfunction
sodium retention

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5
Q

name and location of valves of the heart

A

tricuspid: right atrium to right ventricle
mitral: left atrium to left ventricle
pulmonary: right ventricle to pulmonary artery
aortic: left ventricle to aorta

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6
Q

describe how blood flows through the heart

A

right ventricle –> pulmonary valve –> pulmonary artery –> lungs –> pulmonary vein –> left atrium –> mitral valve –> left ventricle –> aortic valve –> aorta –> organs/tissues –> superior and inferior vena cava –> right atrium –> tricuspid valve –> right ventricle

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7
Q

What are the layers of veins and arteries?

A

tunica externa: outermost layer, loose connective tissue
tunica media: middle layer, smooth muscle
tunica intima: inner most layer, simple squamous epithelium (endothelium) and elastic fibers composed of elastin

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8
Q

how are veins and arteries anatomically different?

A

arteries have more muscles than veins
arteries are more round than veins
veins partially collapse secondary to not being filled to capacity
valves are often present in veins but not in arteries

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9
Q

describe the flow of electrical activity through the heart

A

starts at sinoatrial node (SA)
in the right atrium near the superior vena cava
discharge rate determines heart rate
action potential spreads from right atrium to left atrium
AV node (atrioventricular node) at the base of the right atrium links atrial and ventricular depolarization
right atrium action potential –> depolarization of AV node
Bundle of His (AV bundle) is in the interventricular septum
impulse from AV node –> bundle of His
bundle of His is divided into right bundle branch & left bundle branch which go from septum to walls of right and left ventricle
Purkinje fibers are contacted by RBB and LBB - large conducting cells distribute the impulse to most of the ventricles
contact the non-conducting system (ventricular myocardial cells –> rest of the ventricles)

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10
Q

difference between diastole and systole

A

diastole: heart is at rest
tricuspid and mitral valves are open, aortic and pulmonary valves are closed

systole: heart contracts
tricuspid and mitral valves are closed, pulmonary and aortic valves open

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11
Q

What valve connects the right and atrium and right ventricle?

A

tricuspid valve

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12
Q

describe the RAAS

A

Renin Angiotensin Aldosterone System
when renal blood flow decreases, juxtaglomerular cells convert prorenin (in the blood) to renin and secrete it into circulation.
plasma renin converts angiotensinogen (released by liver) into angiotensin I.
Angiotensin I is converted by ACE (angiotensin converting enzyme - found in the lungs) to angiotensin II
Angiotensin II = vasoconstriction AND stimulates secretion of aldosterone from adrenal cortex
aldosterone tries to increase blood pressure by increasing reabsorption of ions (sodium) and water in the distal tubule & collecting duct in nephron (also causes K+ secretion) to increase water retention
ACE also inactivates bradykinin

IMPORTANT: there are non-renin and non ACE ways to get from angiotensinogen and angiotensin I to angiotensin II

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13
Q

What are the consequences of angiotensin II?

A

AT 1 receptor (where many of the negative consequences are):

  • vascular smooth muscle grown –> increases arteriolar constriction
  • CNS –> stimulated to increase cardiac output (CO)
  • adrenal cortex –> aldosterone stimulation –> increase renal sodium reaborption
  • kidney –> increase filtration fraction –> increase GFR
  • brain –> increase ADH and thirst (trying to hold onto more fluid) –> increase free water intake

AT 2 receptor:

  • vasodilation
  • anti-proliferation
  • cell differentiation
  • tissue repair
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14
Q

What are the consequences of aldosterone?

A
  • heart: myocardial fibrosis, ventricular arrhythmias, left ventricular hypertrophy (LVH)
  • kidney: sodium retention, magnesium & potassium loss
  • vasculature: hypertension, endothelial dysfunction, inhibits nitric oxide synthesis, prothrombotic
  • CNS: sympathetic activation, parasympathetic inhibition
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15
Q

Define:
preload
afterload
stroke volume

A

Preload: pressure stretching the ventricle of the heart after atrial contraction and subsequent passive filling of the ventricle. End diastolic volume.

Afterload: tension or pressure used by the chamber of the heart in order to contract and eject blood out of the chamber. End systolic volume.

Stroke volume: end diastolic volume - end systolic volume (how much blood is actually pumped out of the heart with each beat.

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16
Q

Define:
cardiac output
Cardiac index
Ejection fraction

A

Cardiac output (CO): amount of blood pumped per unit of time = heart rate (HR) X SV

Cardiac index (CI): CO adjusted for BSA. = CO/BSA

Ejection Fraction (EF): fraction of blood ejected by the left ventricle during contraction or ejection phase of cardiac cycle. = SV/EDV X 100%

EDV = end diastolic volume
normal EF is b/t 55-70%
EF heart failure =

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17
Q

Define:
Mean arterial pressure (MAP)
pulmonary capillary wedge pressure (PCWP)

A

Mean arterial pressure (MAP): (CO X systemic vascular resistance [SVR]) + central venous pressure (CVP)
also = [(2 X diastolic pressure) + systolic pressure]/3

Pulmonary capillary wedge pressure (PCWP):
under most circumstances provides an accurate estimate of the diastolic filling (preload) of the left heart
during diastole, when mitral valve is open, the PCWP reflects LVEPD - an index of left ventricular end-diastolic volume (preload)

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18
Q

What is Forrester’s Classification?

A

Uses Cardiac Index (CI) and pulmonary capillary wedge pressure (PCWP)
CI indicates degree of perfusion (warm or cold depending on presence of hypoperfusion) CI of 18 mmHg = wet (volume overload)

Subset I: no hemodynamic compromise, CI > 2.2 L/min/m^2 and PCWP 2.2, PCWP > 18
Subset III: hypoperfusion, cold and dry: CI 18

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19
Q

How do you clinically assess hemodynamics?

A

elevated preload =

  • hepatomegaly
  • jugular venous distension (JVD) visible pulsing of jugular by ear
  • peripheral edema - tends to be bilateral, lower extremity
  • pulmonary crackles (signs of fluid accumulation)
  • S3 heart sound (extra heart sound - associated with heart failure)
  • mucous membranes and skin turgor
  • daily weight

Afterload:

  • vascular diastolic pressure
  • pulse pressure
  • pulses
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20
Q

What is the Swan-Ganz catheter?

A

passing a thin tube into the right side of the heart (through right atrium, right ventricle, to pulmonary artery) to monitor heart’s function and blood flow.
done in people who are critically ill

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21
Q

Define:
arteriosclerosis
atherosclerosis
Ischemic Heart Disease

A

arteriosclerosis: hardening of the arteries
Atherosclerosis: subset of arteriosclerosis. formation of atheroma (fibrous fatty intimal plaques) in arterial walls
Ischemic Heart Disease (IHD): lack of oxygen tension at cellular level, results in loss of high energy phosphates due to disruption of aerobic metabolism: CV dysfunction occurs at cellular level due to imbalance between myocardial oxygen supply and myocardial demand. cellular dysfunction may be transient or permanent (cell death). cellular dysfunction translates into organ dysfunction.
etiology: atherosclerosis
Also referred to as: Coronary heart disease (CHD), coronary artery disease (CAD), atherosclerotic cardiovascular disease (ASCVD)

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22
Q

What are the steps in developing atherosclerosis?

A
  1. endothelial dysfunction
  2. fatty streak formation
  3. fibrous plaque formation
  4. thrombus formation
23
Q

What are some causes of endothelial dysfunction?

A 
obesity, diabetes, smoking 
age,
sex (male > female)
family history of CHD
dyslipidemia (increase cholesterol, decrease HDL-C)
HTN
increased homocysteine
24
Q

Where does endothelial dysfunction occur?

A

only in tunica intima

25
Q

What is the definition of endothelial dysfunction and what are the results?

A

diminished ability of the endothelium to regulate vascular tone, clotting and inflammation
resulting in vasoconstriction, pro-thrombotic and pro-inflammatory
angiotensin II and endothelin produced as a result of the dysfunctional endothelium resulting in vasoconstriction

26
Q

What happens in fatty streak formation?

A

asymptomatic
yellow streak of lipid-filled macrophage foam cells (initial lesion of atherosclerosis)
inside artery wall, monocytes differentiate into macrophages
macrophages engulf lipoproteins (like LDL) and then form foam cells
both macrophages and foam cells secrete growth factors & cytokines resulting in: cell proliferation, inflammation, matrix degradation

27
Q

What happens in fibrous plaque formation?

A

can be asymptomatic or symptomatic depending on stage & amount of plaque development
whitish yellow lump occluding lumen of coronary arteries, aorta and carotids
process:
foam cells accumulate and expand into lining of artery wall
smooth muscle cells from the middle layer of the artery (media) move into the layer of endothelial cells (intima) to stabilize the vulnerable plaque area
plaque grows and protrudes into the lumen of the blood vessel
a fibrous cap of connective tissue overlays the fibrous plaque

28
Q

what is the primary cause of hardened and narrowed arteries (atherosclerosis)?

A

stable plaque: thick calcified cap & smaller fatty core.
(vs. unstable plaque which has a thin calcified cap covering a larger fatty core - more likely to rupture which can trigger a heart attack or stroke).

29
Q

What happens in thrombus formation?

A

symptomatic
either complete or partial vessel occlusion resulting in a mismatch of oxygen supply and demand
Process:
when the fibrous cap ruptures then contents of plaque begin to leak into the lumen of the vessel
this is interpreted by the body as a site of injury & results in platelet being recruited to site
as the platelets aggregate at the site of injury, they form a thrombotic mass (thrombus or clot)
this mass is further stabilized by thrombin the conversion of fibrinogen to fibrin

30
Q

What affects oxygen supply vs oxygen demand?

A

oxygen supply:
coronary blood flow
oxygen extraction
oxygen availability

oxygen demand:
heart rate
contractility
wall tension
(beta blockers and calcium channel blockers decrease oxygen demand)
31
Q

what causes cardiac remodeling and what is it?

A

increased stress and demand can cause remodeling (chronic HTN, for example, can cause left ventricular hypertrophy)
remodeling is the process by which ventricular size, shape & function are regulated by mechanical, neurohormonal and genetic factors. May be due to physiological and adaptive processes during normal growth or pathological damage

32
Q

How are you classified as having clinical atherosclerotic cardiovascular disease (ASCVD)?

A 
Coronary heart disease (CHD)
- acute coronary syndromes
- history of myocardial infarction
- stable or unstable angina
- coronary revascularization
Symptomatic carotid artery disease
- stroke
- transient ischemic attack (TIA)
Peripheral arterial disease or revascularization
33
Q

what are some modifiable risk factors for ASCVD?

A

smoking
HTN
total cholesterol (H = Happy - get it as high as it can be)
Low high-density lipoprotein cholesterol (HDL-C)

34
Q

What are non-modifiable risk factors for ASCVD?

A

gender
race (African Americans have higher risk)
Family history of coronary heart disease (CHD)
- CHD in male 1st degree relative /= 45 y.o.
- female >/= 55 y.o.

35
Q

how does ischemic heart disease present clinically?

A

sudden cardiac death due to electrical instability
angina
- substernal chest “pressure” sensation
- radiation of discomfort to shoulder, back, arm or neck
- predictable pattern - brought on by exertion, relieved with rest or medication
- short duration: 1-15 minutes

36
Q

What is acute coronary syndrome?

A
  • Unstable angina: new onset angina, changing pattern of angina or worsening (usually longer duration of discomfort), angina at rest or with decreasing effort, post infarction angina
  • acute myocardial infarction: ST - elevation or non-ST-elevation, Death - 50% of patients w/acute MI die before reaching hospital, chest discomfort prolonged more than 30 minutes & not relieved with nitroglycerin, atypical symptoms: dyspnea, nausea/vomiting, pronounced fatigue; asymptomatic: 1/3 of patients w/acute MI have no symptoms, EKG changes of acute MI, laboratory changes of acute MI (CPK, Troponin)
37
Q

what are some measures that may stabilize atheroma?

A 
decrease LDL
increase HDL
decrease angiotensin II
decrease insulin resistance
decrease oxidative stress
decrease blood pressure
38
Q

what are some clinical consequences of atherosclerosis?

A

brain arteries:

  • stroke
  • TIA

coronary arteries:

  • stable angina
  • unstable angina
  • MI

leg arteries:
- peripheral artery/vascular disease

39
Q

What are the classifications of obesity?

A

underweight: BMI /= 40

40
Q

What is an EKG (ECG)?

A 
measures electrical activity of the heart
represents the sum total of electrical vectors arising from myocardial cells as they depolarize and repolarize
gives information on:
- heart rate
- heart rhythm
- conduction times
- ischemia
- infarction (acute and old)
- hypertrophy

NON-invasive

41
Q

What is a holder Monitor?

A

Ambulatory EKG
used to evaluate baseline heart rhythms
typically ordered to evaluate symptoms of palpitations, dizziness or syncope
recording durations typically last 24-48 hours
asymptomatic rhythm disorders that are common:
- premature ventricular contractions (PVC’s)
- premature atrial contractions (PAC’s)
- sinus bradycardia (HR 110/min)

42
Q

What is echocardiography?

A

non-invasive
realtime 2 dimensional imaging of the heart
measurement of left ventricular function, vavular morphology and valve function
can be combined with exercise or dopabutamine stress to evaluate inducable regional left ventricular wall motion abnormalities (surrogate marker for ischemia)
echo probe can be endoscopically placed into the esophagus to obtain more detailed information regarding valvular morphology and/or cardiac shunts
- transesophageal echo = TEE (more invasive)
- tranthroacic echo = TTE (across the chest)

43
Q

why would you do an exercise stress test?

A
  • diagnosis of obstructive CAD (coronary artery disease)
  • risk assessment & prognosis in patients with symptoms or a prior history of CAD
  • post MI risk assessment and prognosis
  • special groups: asymptomatic patients, post revascularization patients, rhythm disorders, women (b/c they tend to have more asymptomatic CVD than men
44
Q

what is exercise testing?

A

treadmill or bicycle ergometer: standard EKG stress test, exercise echocardiography, exercise nuclear imaging (thallium or technitium)
exercise used to increase myocardial oxygen demand: increase heart rate, increase blood pressure
limited if patient cannot exercise to adequate level (85% maximal predicated heart rate
max predicted heart rate = 220 - age
chronotropic incompetence may be secondary to drugs (beta blockers)

45
Q

What are advantages of exercise stress testing?

A
  • low cost
  • wide availability
  • patient acceptability
  • exercise capacity determined
  • convenience
46
Q

what are disadvantages of exercise stress testing?

A
  • limited sensitivity and specificity
  • does not localize ischemia
  • no estimate of LV function
  • requires cooperation and ability to walk
47
Q

How can we pharmacologically stress test?

A 
non-invasive
Ischemic test (inotropes)
- induction of true ischemia resulting in regional wall motion abnormalities
- dobutamine
- arbutamine

Perfusion stress (vasodilators)

  • induction of coronary steal results in decreased coronary flow and evaluated as a surrogate for ischemia
  • dipyridamole
  • adenosine
48
Q

When do you use a Coronary Artery Calcium (CAC) Score?

A

non-invasive
reasonable for ASCVD risk assessment in asymptomatic adults
- intermediate risk: ASCVD risk 10-20%
- low to intermediate risk: ASCVD risk 6-10%

not recommended for ASCVD risk assessment in asymptomatic adults
- low risk: ASCVD risk

49
Q

What is a carotid artery intima-media thickness (CIMT)

A

less common in clinical practice, more common in studies
ultrasound image of carotid artery walls
reasonable for ASCVD risk assessment in asymptomatic adults at intermediate risk
non-invasive

50
Q

What is coronary angiography?

A

invasive
- an x-ray examination of the blood vessels or chambers of the heart
- a catheter is inserted into a blood vessel in your upper thigh (groin area) or arm
- the tip of the tube is positioned either in the heart or at the beginning of the arteries supplying the heart, and a special fluid (called a contrast medium or dye) is injected
- this fluid is visible by x-ray, and the pictures that are obtained are called angiograms
-used diagnostically to document presence & severity of disease
use when: suspected CAD, high risk features with exercise stress test (early & significant change on ECG during test > 2mm), multiple lead involvement on ECG, prolonged recovery from ischemia, low workload performance, abnormal blood pressure response (decreased bp), ventricular arrhythmias
- not recommended in asymptomatic individuals

51
Q

What is coronary CT angiography (CCTA)?

A
  • no catheter threated through your blood vessels to your heart like traditional coronary angiograms
  • x-ray machine to produce images of your heart & its blood vessels
  • noninvasive & don’t require any recovery time
  • both CT and traditional coronary angiograms expose you to radiation
  • known CAD: traditional coronary angiogram may be a better option, since you can also receive treatment PCl if needed at time of procedure
52
Q

What is coronary angioplasty/percutaneous coronary intervention? (PCl)

A
  • angioplasty involves temporarily inserting & expanding a tiny balloon at the site of blockage to help widen narrowed artery
  • angioplasty is usually combined with implantation of a small metal coil (stent) in the clogged artery to help prop it open & decrease the chance of it narrowing again
  • angioplasty/PCl are used to open clogged heart arteries
  • Coronary angioplasty can improve symptoms associated with blocked arteries such as chest pain & shortness of breath, and can be used during a heart attack to quickly open a blocked artery & minimize heart damage
  • Used for: acute MI, significant CAD with obstruction, significant angina symptoms (unstable angina)
53
Q

What is coronary artery bypass surgery? (CABG)

A

reroutes, or bypasses blood around clogged arteries to improve blood flow & oxygen to the heart

  • mid-sternotomy incision
  • vein graft harvest & placement (long leg vein may be taken, one end sewn above the blocked area & the other end grafted to coronary artery below blocked area, artery may be detached from chest wall & open end attached to coronary artery below the blocked area, patient may undergo 1,2,3 or more bypass grafts, depending on how many coronary arteries are blocked
  • cardiopulmonary bypass with a pump oxygenator (heart-lung machine) is used for most coronary bypass graft operation
  • during past several years, more surgeons have started performing off-pump coronary artery bypass surgery (OPCAB)
  • increases bood flow to heart muscle & can relieve chest pain & reduce risk of heart attack
  • used when left main coronary artery is stenosed, 2 - 3 vessel CAD, medically refractory angina not amenable to PCl

Pharmacotherapy 2/3 (7 decks)

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